Obstructive sleep apnea and impaired glucose metabolism.

Transcription

1 Abstract collection. Obstructive sleep apnea and impaired glucose metabolism. Issue 2, April 2011 With an introduction by Michiel M.M. Eijsvogel, MD

2 Contents 03 Contents. Obstructive sleep apnea and impaired glucose metabolism. 02 Introduction. Michiel M.M. Eijsvogel. 04 References. Abstracts. 06 Obstructive sleep apnea as a risk factor for type 2 diabetes. Botros N, Concato J, Mohsenin V, Selim B, Doctor K, Yaggi HK. 07 Obstructive sleep apnea: role in the risk and severity of diabetes. Pamidi S, Aronsohn RS, Tasali E. 08 Prevalence and recognition of obstructive sleep apnea in Chinese patients with type 2 diabetes mellitus. Lam DC, Lui MM, Lam JC, Ong LH, Lam KS, Ip MS. 09 Obstructive sleep apnoea syndrome and the metabolic syndrome in an internal medicine setting. Angelico F, del Ben M, Augelletti T, de Vita R, Roma R, Violi F, Fabiani M. 10 Nocturnal intermittent hypoxia and the development of type 2 diabetes: the Circulatory Risk in Communities Study (CIRCS). Muraki I, Tanigawa T, Yamagishi K, Sakurai S, Ohira T, Imano H, Kitamura A, Kiyama M, Sato S, Shimamoto T, Konishi M, Iso H; CIRCS Investigators. 11 Impact of untreated obstructive sleep apnea on glucose control in type 2 diabetes. Aronsohn RS, Whitmore H, Van Cauter E, Tasali E. 12 Impact of gender on incident diabetes mellitus in obstructive sleep apnea: a 16-year follow-up. Celen YT, Hedner J, Carlson J, Peker Y. 13 A randomised controlled trial of nasal continuous positive airway pressure on insulin sensitivity in obstructive sleep apnoea. Lam JC, Lam B, Yao TJ, Lai AY, Ooi CG, Tam S, Lam KS, Ip MS.

3 04 Introduction Introduction 05 Obstructive sleep apnea and impaired glucose metabolism. Introduction. Growing evidence indicates that impaired glucose metabolism and obstructive sleep apnoea (OSA) are linked, even after correction for co-existing factors such as obesity, hypertension and dyslipidaemia. Because both diseases share common risk factors, OSA patients show a higher incidence of diabetes mellitus (DM) and, contrarily, DM patients a higher incidence of OSA. Given the high prevalence of diabetes mellitus in OSA and vice versa, the increased cardiovascular risk and the treatability of these conditions, it is extremely important that both patients and physicians be aware of these interrelationships. Michiel M.M. Eijsvogel, MD Michiel M.M. Eijsvogel, MD Pulmonary Physician Medisch Spectrum Twente Hospital, Enschede, Netherlands The metabolic disorders that commonly coexist with OSA can be measured by impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), both linked to insulin resistance or shortage. For example, the Sleep Heart Health study 1 on 2,656 community-dwelling subjects found that glucose intolerance was dose-dependently related to the apnoea-hypopnoea index (AHI) and hypoxemia even after correction for obesity, age and gender. In 400 Swedish females corrected for age, obesity, alcohol consumption, smoking and physical activity, the AHI was associated with increased insulin levels 2. Thus, OSA appears independently associated with glucose intolerance and insulin resistance and may lead to type II DM. Several recent studies have examined this relationship by adjusting for obesity and other confounding factors (like BMI, weight change, waist circumference, age, sex, race, hypertension, etc). In a Wisconsin sleep cohort 3, this adjusted change for DM in OSA (AHI>15) patients was 2.3 (CI ), but an independent relationship at 4 years follow-up was not statistically proven. Botros et al. 4 examined 1233 consecutive patients evaluated for sleep-disordered breathing; 544 without DM were followed for 5 years. Their adjusted incidence for developing DM was 1.43 (CI ). The authors also found that CPAP treatment of severe OSA reduced the chance for developing DM. Ronksley et al. 5 did a crosssectional analysis of 2149 patients referred for sleep-disordered breathing. DM was defined by self-reporting and the concurrent use of anti-diabetics. The authors observed a dosedependent relationship between AHI and risk for DM; DM occurred in 4.4%, 5.5%, 7.4% and 15.3% of the non-osa, mild, moderate and severe OSA groups, respectively. However, only severe OSA (AHI>30) was associated with DM (odds ratio 2.18) after adjusting for confounders. After stratification for excessive daytime sleepiness (EDS), ESS 10), this relationship was only found in severe OSA patients (odds ratio 2.59; CI ) and may be explained by an association between EDS and sleep disruption. Studies on healthy volunteers have shown that sleep disruption leads to over-activity of the sympathetic nervous system, raised cortisol levels and glucose intolerance 6,7. In the Australian town of Busselton, 295 persons were investigated twice for OSA and DM at 4- to 5-year intervals 8. The incidence of new DM after 4 5 years with full adjustment for confounders was 2.2% in non-osa, 3.4% in mild and 20% moderate/severe OSA patients. Thus, at least severe OSA appears to be a risk factor for type II DM. The occurrence of OSA in DM and OSA cohorts (AHI>5) can reach 80% when hypertension or severe obesity are included. In the USA Sleep AHEAD study 9 where 305 DM-type II patients with a mean BMI = 36 underwent full polysomnography at home, 86% had at least mild OSA (AHI>5) and 22% severe OSA (AHI>30). In most of these patients waist circumference predicted OSA and BMI predicted severe OSA. The prevalence of moderate to severe OSA defined as AHI>20 in 2,668 Swedish hypertensive patients was 36% in the diabetic subgroup compared to 14% in the normoglycaemic group. A significant relationship to glycaemic control was also found 10. Lam et al. 11 estimated a prevalence of OSA (AHI>5) to be 17.5% in type II diabetics with stable medical illnesses; Aronsohn 12 but not Lam 11 found an association between glycaemic control (HbA1c) and sleep indices. These and other studies all found that the risk of OSA was higher in type II diabetics than in the general population. Grunstein et al. 13 investigated the long-term effects of bariatric surgery in patients with severe obesity. The mean BMI decreased by 9.7 kg/m 2 and 0 in patients vs. controls. Compared to the controls, the persisting snoring and apnoea-adjusted odds ratio was 0.14 and 0.16, respectively. Compared to subjects without apnoea at follow-up (n=2,453), subjects who continued to have or developed apnea (n=404) showed a higher incidence of diabetes (adjusted odds 2.3). Dawson et al. 14 monitored glucose during sleep in 20 patients with newly diagnosed OSA and type II DM before and after 3 months CPAP therapy. The mean glucose level and the difference between maximum and minimum glucose levels all decreased significantly on CPAP, thus suggesting better and more stable DM control with CPAP. Two randomized controlled trials (RCT) with CPAP and sham CPAP on DM type II 15 and non-dm 16, respectively, showed no change in fasting glucose levels, insulin resistance or HbA 1c after CPAP treatment. However, CPAP compliance was just above (Coughlin 4.2 hours) or clearly below (West 3.6 hours) the minimum advised use of 4 hours per night. Babu et al. 17 studied 24 patients with DM and OSA on CPAP and found a reduction in HbA 1c levels that was strongly correlated with CPAP use. In this non-randomized study, the mean CPAP use was 6.6 hours per night. In a recent RCT 11, 61 males with OSA but no significant comorbidities received CPAP or sham CPAP for 1 and 12 weeks. Increased insulin sensitivity was only noted in the therapeutic CPAP group. At 12 weeks this improvement persisted in the modestly obese (BMI > 25) but not in the nonobese (BMI <25) group. The studies discussed confirm a common co-existence of OSA and impaired glucose metabolism. An awareness of this can lead to better treatment modalities and possibly prevention in the general population.

4 06 References References 07 References. 1. Punjabi NM, Shahar E, Redline S, Gottlieb DJ, Givelber R, Resnick HE. Sleep-disordered breathing, glucose intolerance and insulin resistance. The Sleep Heart Health Study. Am J Epidemiol 2004; 160: Theorell-Haglöw J, Berne C, Janson C, Lindberg E. Obstructive sleep apnoea is associated with decreased insulin sensitivity in females. Eur Respir J 2008; 31: Reichmuth KJ, Austin D, Skatrud JB, Young T. Association of sleep apnea and type II diabetes: a population based study. Am J Respir Crit Care Med 2005; 172: Botros N, Concato J, Mohsenin V. Obstructive sleep apnea as a risk factor for type 2 diabetes. Am J Med 2009; 122: Ronksley PE, Hemmelgarn BR, Heitman SJ, Hanly PJ, Faris PD, Quan H, Tsai WH. Obstructive sleep apnoea is associated with diabetes in sleepy subjects. Thorax 2009; 64: Spiegel K, Leproult R, Cauter E. Impact of sleep debt on metabolic and endocrine function. Lancet 1999; 354: Strohl KP, Boehm KD, Denko CW, Novak RD, Decker MJ. Biochemical morbidity in sleep apnea. Ear Nose Throat J 1993; 72: Marshall NS, Wong KK, Phillips CL, Liu PY, Knuiman MW, Grunstein RR. Is sleep apnea an independent risk factor for prevalent and incident diabetes in the Busselton Health Study? J Clin Sleep Med 2009; 5: Foster GD, Sanders MH, Millman R, Zammit G, Borradaile KE, Newman AB, Wadden TA, Kelley D, Wing RR, Sunyer FX, Darcey V, Kuna ST, Sleep AHEAD Research Group. Obstructive sleep apnea among patients with type 2 diabetes. Diabetes Care 2009; 32: Elsmasry A, Lindberg E, Berne C, Gislason T, Awad Tageldin M, Boman G. Sleep-disordered breathing and glucose metabolism in hypertensive men: a population-based study. J Intern Med 2001; 249: Lam JC, Lam B, Yao TJ, Lai AY, Ooi CG, Tam S, Lam KS, Ip MS. A randomised controlled trial of nasal continuous positive airway pressure on insulin sensitivity in obstructive sleep apnoea. Eur Respir J 2010; 35: Aronsohn RS, Whitmore H, Van Cauter E, Tasali E. Impact of untreated obstructive sleep apnea on glucose control in type 2 diabetes. Am J Respi Crit Care Med 2010; 181: Grunstein RR, Stenlöf K, Hedner JA, Peltonen M, Karason K, Sjöström L. Two year reduction in sleep apnea symptoms and associated diabetes incidence after weight loss in severe obesity. Sleep 2007; 30: Dawson A, Abel SL, Loving RT, Dailey G, Shadan FF, Cronin JW, Kripke DF, Kline LE. CPAP therapy of obstructive sleep apnea in type 2 diabetics improves glycemic control during sleep. J Clin Sleep Med 2008; 4: West SD, Nicoll DJ, Wallace TM, Matthews DR, Stradling JR. Effect of CPAP on insulin resistance and HbA 1c in men with obstructive sleep apnoea and type 2 diabetes. Thorax 2007; 62: Coughlin SR, Mawdsley L, Mugarza JA, Wilding JP, Calverley PM. Cardiovascular and metabolic effects of CPAP obese males with OSA. Eur Respir J 2007; 29: Babu AR, Herdegen J, Fogelfeld L, Shott S, Mazzone T. Type 2 diabetes, glycemic control, and continuous positive airway pressure in obstructive sleep apnea. Arch Intern Med 2005; 165:

5 08 Abstracts Abstracts 09 Abstract. Obstructive sleep apnea as a risk factor for type 2 diabetes. Abstract. Obstructive sleep apnea: role in the risk and severity of diabetes. Botros N, Concato J, Mohsenin V, Selim B, Doctor K, Yaggi HK. Division of Pulmonary, Critical Care, and Sleep Medicine, Yale University School of Medicine, New Haven, Conn., USA Am J Med Dec;122(12): PURPOSE: Cross-sectional studies have documented the co-occurrence of obstructive sleep apnea (hereafter, sleep apnea) with glucose intolerance, insulin resistance, and type 2 diabetes mellitus (hereafter, diabetes). It has not been determined, however, whether sleep apnea is independently associated with the subsequent development of diabetes, accounting for established risk factors. METHODS: This observational cohort study examined 1233 consecutive patients in the Veteran Affairs Connecticut Healthcare System referred for evaluation of sleep-disordered breathing; 544 study participants were free of preexisting diabetes and completed a full, attended, diagnostic polysomnogram. The study population was divided into quartiles based on severity of sleep apnea as measured by the apnea-hypopnea index. The main outcome was incident diabetes defined as fasting glucose level >126 mg/ dl and a corresponding physician diagnosis. Compliance with positive airway pressure therapy, and its impact on the main outcome, also was examined. RESULTS: In unadjusted analysis, increasing severity of sleep apnea was associated with an increased risk of diabetes (P for linear trend <.001). After adjusting for age, sex, race, baseline fasting blood glucose, body mass index, and weight change, an independent association was found between sleep apnea and incident diabetes (hazard ratio per quartile 1.43; confidence interval ). Among patients with more severe sleep apnea (upper 2 quartiles of severity), 60% had evidence of regular positive airway pressure use, and this treatment was associated with an attenuation of the risk of diabetes (logrank test P=.04). CONCLUSION: Sleep apnea increases the risk of developing diabetes, independent of other risk factors. Among patients with more severe sleep apnea, regular positive airway pressure use may attenuate this risk. PMID: [PubMed - indexed for MEDLINE] Pamidi S, Aronsohn RS, Tasali E. Department of Medicine, The University of Chicago, 5841 South Maryland Avenue, MC 4000, Chicago, IL 60637, USA. Best Pract Res Clin Endocrinol Metab Oct;24(5): Obstructive sleep apnea (OSA) is a treatable sleep disorder that is pervasive among overweight and obese individuals. Current evidence supports a robust association between OSA and insulin resistance, glucose intolerance and the risk of type 2 diabetes, independent of obesity. Up to 83% of patients with type 2 diabetes suffer from unrecognized OSA and increasing severity of OSA is independently associated with poorer glucose control. Evidence from animal and human models that mimic OSA supports a potential causal role for OSA in altered glucose metabolism. Robust prospective and randomized clinical trials are still needed to test the hypothesis that effective treatment of OSA may prevent the development of type 2 diabetes and its complications, or reduce its severity. Type 2 diabetes is occurring at alarming rates worldwide and despite available treatment options, the economic and public health burden of this epidemic remains enormous. OSA might represent a novel, modifiable risk factor for the development of prediabetes and type 2 diabetes. PMID:

6 010 Abstracts Abstracts 011 Abstract. Prevalence and recognition of obstructive sleep apnea in Chinese patients with type 2 diabetes mellitus. Abstract. Obstructive sleep apnoea syndrome and the metabolic syndrome in an internal medicine setting. Lam DC, Lui MM, Lam JC, Ong LH, Lam KS, Ip MS. Department of Medicine, Queen Mary Hospital, University of Hong Kong, 102 Pokfulam Rd, Hong Kong, ROC. Chest Nov;138(5): BACKGROUND: Obstructive sleep apnea (OSA) is associated with disorders of glucose metabolism. Previous studies revealed a high prevalence of OSA among subjects with type 2 diabetes mellitus (DM). The aims of this study were to determine the prevalence of OSA and associated clinical factors in Chinese patients with DM. METHODS: All records of the DM clinic at a teaching hospital in Hong Kong were screened between January 2007 and June Inclusion criteria for patients were Chinese, aged 18 to 75 years, with type 2 DM. Patients with unstable medical illnesses, gestational diabetes, or on renal replacement therapy were excluded. RESULTS: Of 3,489 records screened, 1,859 subjects were eligible. A random sample of 663 (mean age, 58.2 ± 10.8; mean BMI, 26.0 ± 4.6), except six with known OSA, were invited for polysomnography (PSG). Of 165 subjects on which PSG was performed, OSA was diagnosed (apnea-hypopnea index [AHI] 5.0/h) in 89 subjects (53.9%, median Epworth Sleepiness Scale, 6 [interquartile range 3, 10]). Fifty-four (32.7%) had moderate/ severe OSA (AHI 15/h). The estimated OSA prevalence in this diabetic cohort was 17.5% (24.7% in men, 10.3% in women). Regression analysis identified that AHI was associated independently with higher BMI, advanced age, male sex, and higher diastolic BP (R(2) = 29.6%). The adjusted OR of requiring three or more antihypertensive drugs in moderate/ severe OSA was 2.48 (95% CI, ). No association between glycemic control (HbA1c) and sleep was identified. CONCLUSIONS: In conclusion, OSA is more prevalent in Chinese adults with DM than in the general population. A high index of suspicion for OSA in patients with DM is warranted, because they may not have overt daytime sleepiness. PMID: [PubMed indexed in MEDLINE] Angelico F, del Ben M, Augelletti T, de Vita R, Roma R, Violi F, Fabiani M. Department of Experimental Medicine, University La Sapienza, Rome, Italy. Eur J Intern Med Jun;21(3): BACKGROUND: Obstructive sleep apnoea syndrome (OSAS) is widely accepted as a cardiovascular risk factor. Lately it has been considered in turn as both a component and one of the causes of the metabolic syndrome (MS). METHODS: We studied 281 heavy snorers of both sexes consecutively attending a metabolic clinic. Aim was to evaluate the association of OSAS and MS in a large series of patients within an internal medicine setting. Patients underwent a clinical and biochemical work up and performed unattended polysomnography. RESULTS: Of 226 non-diabetic snorers, 48 had primary snoring; 54 mild, 51 moderate, and 73 severe OSAS. A positive association was found between OSAS severity, central obesity indices and the mean metabolic score (p=0.016). Prevalence of hypertension increased with OSA severity (p=0.010). Polysomnographic indices were correlated with the metabolic score, insulin levels and central obesity indices. At regression analysis, male sex (t=3.92; p=0.000) and waist circumference (t=3.93; p=0.000) were independently associated with AHI (apnoea/ hypopnoea index), while ODI (oxygen desaturation index) and waist circumference were the independent predictors (t=2.16; p=0.033 and t=3.74; p=0.000 respectively) of the metabolic score. Prevalence of OSA was 83% in 55 patients with diabetes and 34% had severe OSA. Almost all diabetics with OSA had MS. The metabolic score was higher in diabetic OSA as compared to non-diabetic OSAS (p=0.000). CONCLUSIONS: Our findings show a high prevalence of OSAS among patients referred to a metabolic outpatient clinic because of suspected metabolic disorders and heavy snoring and suggest a strong bidirectional association between OSAS and MS. PMID: [PubMed indexed for MEDLINE

7 12 Abstracts Abstracts 13 Abstract. Nocturnal intermittent hypoxia and the development of type 2 diabetes: the Circulatory Risk in Communities Study (CIRCS). Abstract. Impact of untreated obstructive sleep apnea on glucose control in type 2 diabetes. Muraki I, Tanigawa T, Yamagishi K, Sakurai S, Ohira T, Imano H, Kitamura A, Kiyama M, Sato S, Shimamoto T, Konishi M, Iso H; CIRCS Investigators. Public Health, Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka , Japan. Diabetologia Mar;53(3): AIMS/HYPOTHESIS: Although the associations between obstructive sleep apnoea and type 2 diabetes mellitus have been reported in cross-sectional design studies, findings on the prospective association between the two conditions are limited. We examined prospectively the association between nocturnal intermittent hypoxia as a surrogate marker of obstructive sleep apnoea and risk of type 2 diabetes. METHODS: A total of 4,398 community residents aged 40 to 69 years who had participated in sleep investigation studies between 2001 and 2005 were enrolled. Nocturnal intermittent hypoxia was assessed by pulse-oximetry and defined by the number of oxygen desaturation measurements < or =3% per h, with five to <15 per h corresponding to mild and 15 events or more per h corresponding to moderate-to-severe nocturnal intermittent hypoxia, respectively. The development of type 2 diabetes was defined by: (1) fasting serum glucose > or =7.00 mmol/l (126 mg/dl); (2) non-fasting serum glucose > or =11.1 mmol/l (200 mg/ dl); and/or (3) initiation of glucose-lowering medication or insulin therapy. Multivariable model accounted for age, sex, BMI, smoking status, current alcohol intake, community, borderline type 2 diabetes, habitual snoring, excessive daytime sleepiness, sleep duration and (for women) menopausal status. RESULTS: By the end of 2007, 92.2% of participants had been followed up (median follow-up duration [interquartile range] 3.0 [ ] years) and 210 persons identified as having developed diabetes. The multivariableadjusted hazard ratio (95% CI) for developing type 2 diabetes was 1.26 ( ) among those with mild nocturnal intermittent hypoxia and 1.69 ( ) among those with moderate-to-severe nocturnal intermittent hypoxia (p = 0.03 for trend). CONCLUSIONS/INTERPRETATION: Nocturnal intermittent hypoxia was associated with increased risk of developing type 2 diabetes among middle-aged Japanese. PMID: Aronsohn RS, Whitmore H, Van Cauter E, Tasali E. Department of Medicine, MC 1027, University of Chicago, Chicago, IL 60637, USA. Am J Respir Crit Care Med Mar 1;181(5): RATIONALE: Obstructive sleep apnea (OSA), a treatable sleep disorder that is associated with alterations in glucose metabolism in individuals without diabetes, is a highly prevalent comorbidity of type 2 diabetes. However, it is not known whether the severity of OSA is a predictor of glycemic control in patients with diabetes. OBJECTIVES: To determine the impact of OSA on hemoglobin A 1c (HbA 1c ), the major clinical indicator of glycemic control, in patients with type 2 diabetes. METHODS: We performed polysomnography studies and measured HbA 1c in 60 consecutive patients with diabetes recruited from outpatient clinics between February 2007 and August MEASUREMENTS AND MAIN RESULTS: A total of 77% of patients with diabetes had OSA (apnea-hypopnea index [AHI] > or =5). Increasing OSA severity was associated with poorer glucose control, after controlling for age, sex, race, body mass index, number of diabetes medications, level of exercise, years of diabetes and total sleep time. Compared with patients without OSA, the adjusted mean HbA 1c was increased by 1.49% (P = ) in patients with mild OSA, 1.93% (P = ) in patients with moderate OSA, and 3.69% (P < ) in patients with severe OSA (P < for linear trend). Measures of OSA severity, including total AHI (P = 0.004), rapid eye movement AHI (P = 0.005), and the oxygen desaturation index during total and rapid eye movement sleep (P = and P = 0.008, respectively) were positively correlated with increasing HbA 1c levels. CONCLUSIONS: In patients with type 2 diabetes, increasing severity of OSA is associated with poorer glucose control, independent of adiposity and other confounders, with effect sizes comparable to those of widely used hypoglycemic drugs. PMID:

8 14 Abstracts Abstracts 15 Abstract. Impact of gender on incident diabetes mellitus in obstructive sleep apnea: a 16-year follow-up. Abstract. A randomised controlled trial of nasal continuous positive airway pressure on insulin sensitivity in obstructive sleep apnoea. Celen YT, Hedner J, Carlson J, Peker Y. Sleep Medicine Unit, Department of Neurology and Rehabilitation Medicine, Skaraborg Hospital, Skövde, Sweden. J Clin Sleep Med Jun 15;6(3): STUDY OBJECTIVE: To address the influence of gender and obstructive sleep apnea (OSA) on development of diabetes mellitus (DM) in a sleep clinic cohort. DESIGN: A longitudinal observational study. PARTICIPANTS: A consecutive middle-aged (30 69 years) sleep clinic cohort from 1991 (n=318; 254 men, 64 women) with eligible baseline characteristics, clinical charts, and information from the Swedish Hospital Discharge Registry were identified. Ten individuals with DM at baseline and 47 patients who died during the follow-up period were excluded. MEASUREMENTS: The remaining 261 subjects were asked to complete a postal questionnaire regarding concomitant diseases including DM, diagnosed by a physician. RESULTS: In total, 168 patients (64.4%) replied. The incidence of DM was 24.9% in patients with OSA (overnight oxygen desaturations > or =30 in 1991) compared with 10.8% in subjects without OSA (p = 0.020). New-onset DM in men was 19.1% in OSA vs. 11.1% in non- OSA (n.s.), while the corresponding values in women were 50.0% in OSA and 9.5% in non- OSA (p = 0.022). In a multivariate analysis, DM was predicted by OSA in women with an odds ratio (OR) of 11.8, but not by age, body mass index (BMI) at baseline, or weight change at followup. In men, only BMI (OR 1.16) predicted DM. CONCLUSION: The contribution of OSA to DM development seems to be gender-dependent and higher in women than in men. PMID: Lam JC, Lam B, Yao TJ, Lai AY, Ooi CG, Tam S, Lam KS, Ip MS. Dept of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, SAR, China. Eur Respir J Jan;35(1): The effects of treatment of obstructive sleep apnoea (OSA) on glucose metabolism have been investigated previously with conflicting results. This study evaluated the impact of nasal continuous positive airway pressure (ncpap) treatment of OSA on insulin sensitivity. Males with moderate/ severe OSA and no significant comorbidity were randomised to a therapeutic or sham ncpap treatment group for 1 week and then reassessed. Those who received therapeutic ncpap were further evaluated at 12 weeks. Insulin sensitivity (K(itt)) was estimated by the short insulin tolerance test. Other evaluations included blood pressure, metabolic profile, urinary catecholamines and intra-abdominal fat. In total, 61 Chinese subjects were randomised. 31 subjects receiving therapeutic ncpap showed an increase in K(itt) (6.6+/ 2.9 to 7.6+/ 3.2 % x min( 1); p = 0.017), while the 30 patients on sham CPAP had no significant change, and the changes in K(itt) were different between the two groups (p = 0.022). At 12 weeks, improvement in K(itt) was seen in 20 subjects with BMI >or=25 kg x m(-2) (median (interquartile range) 28.3 ( ); p = 0.044), but not in the nine subjects with BMI<25 kg x m(-2), or the entire group. The findings indicate that therapeutic ncpap treatment of OSA for 1 week improved insulin sensitivity in nondiabetic males, and the improvement appeared to be maintained after 12 weeks of treatment in those with moderate obesity. PMID:

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